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Ann Thorac Surg 2008;85:e27-e29. doi:10.1016/j.athoracsur.2008.01.083
© 2008 The Society of Thoracic Surgeons

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How To Do It

Right Ventricular Reduction as an Adjunct Procedure in Tricuspid Valve Repair

Utz Kappert, MDa,*, Sems-Malte Tugtekin, MDb, Ahmed Oudaa, Konstantin Alexiou, MDa, Alexander Schmeisser, MD, PhDb, Steffen Schoen, MDb, Klaus Matschke, MD, PhDa

a Department of Cardiac Surgery, Heart Centre Dresden, University of Technology, Dresden, Germany
b Department of Cardiology, Heart Centre Dresden, University of Technology, Dresden, Germany

Accepted for publication January 28, 2008.

* Address correspondence to Dr Kappert, Heart Centre, University of Technology Dresden Cardiac Surgery, Fetscherstrasse 76, Dresden, D-01307, Germany (Email: u.kappert{at}herzzentrum-dresden.com).


    Abstract
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Functional tricuspid regurgitation secondary to mitral valve disease can not be attributed to the dilatation of the tricuspid annulus alone. Furthermore, geometrical changes of the right ventricle lead to tethering of the tricuspid valve leaflets and thereby to an incomplete leaflet coaptation. With this pathologic entity, conventional isolated tricuspid valve annuloplasty will presumably result in significant residual tricuspid regurgitation. The surgical goal should be the reduction of tricuspid annulus dilatation and annihilation of tethering forces on the tricuspid leaflets. In combination with conventional tricuspid valve annuloplasty, right ventricular reduction surgery, as demonstrated, may be effective in reaching these goals and hereby avoiding residual tricuspid regurgitation in this patient population.


    Introduction
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Functional tricuspid regurgitation (TR) is believed to be caused by tricuspid valve annulus dilatation and tethering of the tricuspid leaflets after severely right ventricular (RV) dilatation. The mechanism underlying functional TR is believed to be multifactorial and related to abnormalities in RV volume, function, and shape.

In patients with RV dilatation, chordal tethering forces on the structurally normal tricuspid leaflets lead to incomplete leaflet coaptation and TR. The RV dilatation also results in tricuspid valve annular dilatation with further TR. Moreover, a concomitant decrease in systolic RV function results in a decrease in systolic closing force of the tricuspid leaflets. Finally, changes in the shape of the RV further exacerbate tricuspid regurgitation [1]. Tricuspid valve annular dilatation and chordal tethering on tricuspid leaflets are the focus of surgical strategies to disrupt this vicious circle.

However, until now success was limited. After conventional tricuspid valve annuloplasty in patients with severe TR and enlarged RV, early postoperative residual TR is obvious in 10% to 39% of cases [2].

To improve the efficacy of tricuspid valve repair in patients with severely enlarged RV, we developed an adjunct surgical procedure to reach the following goals: reduce RV volume, restore RV function, and reshape tricuspid annulus.


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An 80-year-old woman was admitted to our center with dyspnea (New York Heart Association functional class III) as her main complaint. The history revealed chronic atrial fibrillation, diabetes mellitus, hepatic cirrhosis, and a previous cerebrovascular insult without residuum.

A preoperative transesophageal echocardiography revealed severe mitral valve regurgitation, severe TR with an end-diastolic ring dilatation of 27 mm/m2 body surface area in the apical 4-chamber view, and moderate pulmonary hypertension with a right ventricular systolic pressure of 45 mm Hg. The left ventricular ejection fraction was 48%. Magnetic resonance imaging revealed a severely dilated RV with a highly impaired RV ejection fraction (RV end-diastolic volume, 255 mL/m2 body surface area; RV ejection fraction, 22%) with akinetic areas at the right ventricular free wall and tethering of the tricuspid leaflets that was obvious. After exclusion of concomitant coronary artery disease, a mitral valve reconstruction with tricuspid valve annuloplasty was planned.

A median sternotomy was performed and heparin was administered. The RV impressed severely dilated. After aorto-bicaval cannulation, cardiopulmonary bypass was started at normothermia. The aorta was cross clamped and antegrade cold cardioplegia was delivered. The mitral valve reconstruction was performed through a left atriotomy using a 28-mm mitral annuloplasty ring. After forceful injection of saline in the left ventricle using a bulb syringe, there was no residual mitral regurgitation.

Hereafter, the tricuspid valve was exposed through a conventional oblique right atriotomy. The tricuspid valve annulus impressed severely dilated, and annuloplasty of the tricuspid valve was performed using a 32-mm tricuspid annuloplasty ring.

Despite tricuspid valve annuloplasty, there was a severe residual TR revealed by forceful injection of saline in the RV. As a mechanism of the residual TR, leaflet tethering due to right ventricular dilatation was found.

Based on the special anatomical findings of the apparatus of the tricuspid valve, we transformed the "La Place" model to the right heart. With this reduction technique, an approximation of the anterior and posterior papillary muscle is assigned. Consequently, decreased tethering forces on the tricuspid leaflets and a sufficient coaptation level should be achievable.

In preserving the apparatus of the tricuspid valve and preserving the right coronary artery, two strips of felt were placed lengthwise on the epicardial surface of the lateral wall of the right ventricle. Three 2-0 polypropylene sutures were placed as horizontal mattress sutures. The right ventricular wall was plicated to reduce the RV cavum aiming to approximate the papillary muscles (Figs 1–3). Go Go


Figure 1
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Fig 1. (A, B) Intraoperative photographs showing the two strips of felt placed on the right ventricular wall.

 

Figure 2
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Fig 2. Schematic drawing of the right ventricular reduction technique. (A = anterior; P = posterior; RA = right atrium; RCA = right coronary artery; RV = right ventricle; S = septal leaflet of the tricuspid valve.)

 

Figure 3
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Fig 3. (A) Importance of right ventricular and tricuspid valve ring dilatation in the occurrence of functional TR. (B) The arrows indicate the effect of combined tricuspid valve annuloplasty and RV reduction in approximation of tricuspid valve papillary muscles and preventing tethering of tricuspid valve leaflets. (LV = left ventricle; RA = right atrium; RV = right ventricle.)

 
After the procedure, intraoperative transesophageal echocardiography showed no residual TR.

Taking into account the age of the patient and the preoperative multi-morbidity, the postoperative period passed uneventfully. After 3 days of stay in the intensive care unit, the patient was transferred to the normal ward. The New York Heart Association functional class was II. On postoperative day 11, echocardiography showed no residual mitral valve regurgitation or TR. The total hospital stay was 12 days.

A follow-up was done at 1-year. Clinically the patient was in the New York Heart Association functional class I–II and no complications had occurred. Again echocardiography revealed no recurrence of TVR.


    Comment
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 Abstract
 Introduction
 Technique
 Comment
 References
 
In patients with a severely dilated RV, functional TR secondary to mitral valve disease can not be attributed to the dilatation of the TV annulus alone. Furthermore, geometrical changes of the RV may lead to tethering of the tricuspid valve leaflets and thereby to an incomplete leaflet coaptation [1].

Therefore, in patients with this pathologic entity, conventional isolated TV annuloplasty will presumably result in significant residual TR because RV dilatation as an underlying cause of leaflet tethering has not been taken into account [3].

Fukuda and colleagues [2] reported an incidence of severe and moderate residual TR after annuloplasty of 7.4% and 15% in 216 patients, respectively. Also Onoda and colleagues [4] measured postoperative residual moderate TR after Carpentier ring annuloplasty in 29% of 31 patients, whereas McCarthy and colleagues [5] reported a prevalence of severe residual TR in 14% of 790 patients with a risk of reoperation of 4.2% per year.

Regarding the findings of Fukuda and colleagues [2], the preoperative tricuspid annulus diameter was not associated with early outcome after TV annuloplasty, whereas the severity of preoperative TV leaflets tethering, as a measurement of RV dilatation, as well as right and left ventricular dysfunction, predicted significant residual TR after annuloplasty.

Further technical aspects and intraoperative endpoints of RV reduction should be considered.

The initial step of the operation is careful inspection of the right ventricular papillary muscles through the dilated tricuspid annulus. This enables the safe placement of reduction felts to prevent interference with the tricuspid apparatus. From our point of view, incision of the right ventricle should be avoided due to the potential risks of ventriculotomy. Performance of RV reduction is easier and safer with the unloaded RV, which seems to be of particular importance to establish a surgical set up before further modifications are initiated.

Intraoperative endpoints are orientated on echocardiographic data. This concerns the tenting area as well as tricuspid valve function.

Further clinical evaluation is necessary to evaluate if the reduction technique is indicated for exclusive RV surgery. In addition, not only RV dilatation, but also the potential benefit for patients with pulmonary hypertension should be taken into consideration for this additional operative procedure.

Besides clinical data, we will initiate an experimental approach to assess the effects of RV reduction.

In conclusion, in patients with functional TR and severely dilated RV, the surgical goal should be the reduction of tricuspid annulus dilatation and annihilation of tethering forces on the tricuspid leaflets. In combination to conventional tricuspid valve annuloplasty, RV reduction surgery, as demonstrated, may be effective in reaching these goals and hereby avoiding residual TR in this patient population.


    References
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 Abstract
 Introduction
 Technique
 Comment
 References
 

  1. Kim HK, Kim YJ, Park JS, et al. Determinants of the severity of functional tricuspid regurgitation Am J Cardiol 2006;98:236-242.[Medline]
  2. Fukuda S, Gillinov AM, McCarthy PM, et al. Determinants of recurrent or residual functional tricuspid regurgitation after tricuspid annuloplasty Circulation 2006;114(Suppl 1):I582-I587.[Medline]
  3. Fukuda S, Gillinov AM, Song JM, et al. Echocardiographic insights into atrial and ventricular mechanisms of functional tricuspid regurgitation Am Heart J 2006;152:1208-1214.[Medline]
  4. Onoda K, Yasuda F, Takao M, et al. Long-term follow-up after Carpentier-Edwards ring annuloplasty for tricuspid regurgitation Ann Thorac Surg 2000;70:796-799.[Abstract/Free Full Text]
  5. McCarthy PM, Bhudia SK, Rajeswaran J, et al. Tricuspid valve repair: durability and risk factors for failure J Thorac Cardiovasc Surg 2004;127:674-685.[Abstract/Free Full Text]



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